During fiscal year 2011, we accomplished the following: 1. Completed studies on the mechanism of COX2 inhibitors in regulating cell death and inflammation. Our observations demonstrate that celecoxib accentuates apoptosis of activated CD4+ T cell blasts via a COX2-dependent pathway. In contrast, celecoxib inhibits expression pro-inflammatory TNF super-family receptors and ligands via a COX2-independent pathway. The anti-inflammatory effects of celecoxib are mediated via suppression of the NF-&#954;B family member, Rel. Accordingly, Rel-deficient CD4+ T cell blasts resemble celecoxib-treated blasts in many respects. 2. We further extended the celecoxib studies described above to test four additional COX2 inhibitors. Two of these inhibitors affected cell death and interfered with Rel induction as noted for celecoxib, whereas the other two had no effect on Rel-induction or expression of TNF superfamily receptors and ligands. These observations indicate that a major mechanism of anti-inflmmatory effects of coxibs is via suppression of Rel.